50
years ago, in the first phase of marketing the polyunsaturated fatty
acids (PUFA), linoleic acid was “heart protective,” and the saturated
fats raised cholesterol and caused heart disease.

In
the second phase, the other “essential fatty acid,” linolenic acid,
was said to be even better than linoleic acid.

In
the third phase, the longer chain omega -3 (omega minus three, or n
minus three) fatty acids, DHA and EPA, are said to be even better than
linolenic acid.

Along
the way, the highly unsaturated arachidonic acid, which we and other
animals make out of the linoleic acid in foods, was coming to be identified
with the “harmful animal fats.” But we just didn't hear much about
how the amount of arachidonic acid in the tissues depended on the amount
of linoleic acid in the diet.

U.S.
marketing dominates the world economy, including of course the communication
media, so we shouldn't expect to hear much about the role of PUFA in
causing cancer, diabetes, obesity, aging, thrombosis, arthritis and
immunodeficiency, or to hear about the benefits of the saturated fats.

The
saturated fats include the “tropical fats,” because they are synthesized
in very warm organisms, and are very stable at those temperatures. Their
stability offers some protection against the unstable PUFA.

Several
of the degenerative conditions produced by the “essential fatty acids”
can be reversed by use of saturated fats, varying in length from the
short chains of coconut oil to the very long chains of waxes.

=========================================

When
a person uses a drug, there is generally an awareness that the benefit
has to be weighed against the side effects. But if something is treated
as a “nutrient,” especially an “essential nutrient,” there is
an implication that it won't produce undesirable side effects.

Over
the last thirty years I have asked several prominent oil researchers
what the evidence is that there is such a thing as an “essential fatty
acid.” One professor cited a single publication about a solitary sick
person who recovered from some sickness after being given some unsaturated
fat. (If he had known of any better evidence, wouldn't he have mentioned
it?) The others (if they answered at all) cited “Burr and Burr, 1929.” Thesurprising
thing about that answer is that these people can consider any nutritional
research from 1929 to be definitive. It's very much like quoting a 1929
opinion of a physicist regarding the procedure for making a hydrogen
bomb. What was known about nutrition in 1929? Most of the B vitamins
weren't even suspected, and it had been only two or three years since
“vitamin B” had been subdivided into two factors, the “antineuritic
factor,” B1, and the “growth factor,” B2.
Burr had no way of really understanding what deficiencies or toxicities
were present in his experimental diet.

A
few years after the first experiments, Burr put one of his “essential
fatty acid deficient” rats under a bell jar to measure its metabolic
rate, and found that the deficient animals were metabolizing 50% faster
than rats that were given linoleic and linolenic acids as part of their
diet. That was an important observation, but Burr didn't understand
its implications. Later, many experiments showed that the polyunsaturated
fats slowed metabolism by profoundly interfering with the function of
the thyroid hormone and the cellular respiratory apparatus. Without
the toxic fats, respiratory energy metabolism was very intense, and
a diet that was nutritionally sufficient for a sluggish animal wouldn't
necessarily be adequate for the vigorous animals.

Several
publications between 1936 and 1944 made it very clear that Burr's basic
animal diet was deficient in various nutrients, especially vitamin B6.
The disease that appeared in Burr's animals could be cured by fat free
B-vitamin preparations, or by purified vitamin B6 when it became available.
A zinc deficiency produces similar symptoms,
and at the time Burr did his experiments, there was no information on
the effects of fats on mineral absorption. If a diet is barely
adequate in the essential minerals, increasing the metabolic rate, or
decreasing intestinal absorption of minerals, will produce mineral deficiencies
and metabolic problems.

Although
“Burr's disease” clearly turned out to be a B-vitamin deficiency,
probably combined with a mineral deficiency, it continues to be
cited as the basis justifying the multibillion dollar industry that
has grown up around the “essential” oils.

Two
years before Burr's experiment, German researchers found that a fat-free
diet prevented almost all spontaneous cancers in rats. Later work showed
that the polyunsaturated fats both initiate and promote cancer. With
that knowledge, the people who kept claiming that “linoleic, linolenic,
and maybe arachidonic acid are the essential fatty acids,” should
have devoted some effort to finding out how much of that “essential
nutrient” was enough, so that people could minimize their consumption
of the carcinogenic stuff.

Between
the first and second world wars, cod liver oil was recommended as a
vitamin supplement, at first as a source of vitamin A, and later as
a source of vitamins A and D. But in the late 1940s, experimenters used
it as the main fat in dogs' diet, and found that they all died from
cancer, while the dogs on a standard diet had only a 5% cancer mortality.
That sort of information, and the availability of synthetic vitamins,
led to the decreased use of cod liver oil.

But
around that time, the seed oil industry was in crisis because the use
of those oils in paints and plastics was being displaced by new compounds
made from petroleum. The industry needed new markets, and discovered
ways to convince the public that seed oils were better than animal fats.
They were called the “heart protective oils,” though human studies
soon showed the same results that the animal studies had, namely, that
they were toxic to the heart and increased the incidence of cancer.

The
“lipid hypothesis” of heart disease argued that cholesterol in the
blood caused atherosclerosis, and that the polyunsaturated oils lowered
the amount of cholesterol in the blood. Leaving behind the concept of
nutritional essentiality, this allowed the industry (and their academic
supporters, such as Frederick Stare at Harvard) to begin promoting the
oils as having drug-like therapeutic properties. Larger amounts of polyunsaturated
fat were supposed to be more protective by lowering the cholesterol,
and were to be substituted for the saturated fats, which supposedly
raised cholesterol and increased heart disease, producing atherosclerotic
plaques in the blood vessels and increasing the formation of blood clots.

Since
all ordinary foods contain significant amounts of the polyunsaturated
fats, there was no reason to think that, even if they were essential
nutrients, people were likely to become deficient in them. So the idea
of treating the seed oils as drug-like substances, to be taken in large
amounts, appealed to the food oil industry.

Prostaglandins,
which are produced in the body by oxidizing the polyunsaturated fatty
acids, provided an opportunity for the drug industry to get involved
in a new market, and the prostaglandins offered a new way of arguing
for the nutritional essentiality of linoleic and related acids: A whole
system of “hormones” is made from these molecules. Since some
of the prostaglandins suppress immunity, cause inflammation and promote
cancer growth, some people have divided them into the “good prostaglandins”
and the “bad prostaglandins.”

PGI2,
or prostacyclin, is considered to be a good prostaglandin, because it
causes vasodilatation, and so drug companies have made their own synthetic
equivalents:Epoprostenol,
iloprost, taprostene, ciprostene, UT-15, beraprost, and cicaprost. Some
of these are being investigated for possible use in killing cancer.

But
many very useful drugs that already existed, including cortisol and
aspirin, were found to achieve some of their most important effects
by inhibiting the formation of the prostaglandins. It was the body's
load of polyunsaturated fats which made it very susceptible to inflammation,
stress, trauma, infection, radiation, hormone imbalance, and other fundamental
problems, and drugs like aspirin and cortisone, which limit the activation
of the stored “essential fatty acids,” gain their remarkable range
of beneficial effects partly by the restraint they impose on those stored
toxins.

Increasingly,
the liberation of arachidonic acid from tissues during stress is seen
as a central factor in all forms of stress, either acute (as in burns
or exercise) or chronic (as in diabetes or aging). And, as the fat stores
become more toxic, it seems that they more readily liberate the free
fatty acids. (For example, see Iritani, et al., 1984)

During
this same period, a few experimenters were finding that animals which
were fed a diet lacking the “essential” fatty acids had some remarkable
properties: They consumed oxygen and calories at a very high
rate, their mitochondria were unusually tough and stable, their tissues
could be transplanted into other animals without provoking immunological
rejection, and they were very hard to kill by trauma and a wide variety
of toxins that easily provoke lethal shock in animals on the usual diet.
As the Germans had seen in 1927, they had a low susceptibility to cancer,
and new studies were showing that they weren't susceptible to various
fibrotic conditions, including alcoholic liver cirrhosis.

In
1967 a major nutrition publication, Present Knowledge in Nutrition,
published Hartroft and Porta's observation that the “age pigment,”
lipofuscin, was formed in proportion to the amount of polyunsaturated
fat and oxidants in the diet. The new interest in organ transplantation
led to the discovery that the polyunsaturated fats prolonged graft survival,
by suppressing the immune system. Immunosuppression was considered to
have a role in the carcinogenicity of the “essential” fatty acids.

Around
the same time, there were studies that showed that unsaturated fats
retarded brain development and produced obesity.

Substances
very much like the prostaglandins, called isoprostanes and neuroprostanes,
are formed spontaneously from highly unsaturated fatty acids, and are
useful as indicators of the rate of lipid peroxidation in the body.
Most of the products of lipid peroxidation are toxic, as a result of
their reactions with proteins, DNA, and the mitochondria. The age-related
glycation products that are usually blamed on sugar, are largely the
result of peroxidation of the polyunsaturated fatty acids.

Through
the 1970s, this sort of information about the harmful effects of the
PUFA was being slowly assimilated by the culture, though many dietitians
still spoke of “the essential fatty acids, vitamin F.” By 1980,
it looked as though responsible researchers would see the promotion
of cancer, heart disease, mitochondrial damage, hypothyroidism and immunosuppression
caused by the polyunsaturated fats as their most important feature,
and would see that there had never been a basis for believing that they
were essential nutrients.

But
then, without acknowledging that there had been a problem with the doctrine
of essentiality, fat researchers just started changing the subject,
shifting the public discourse to safer, more profitable topics. The
fats that had been called essential, but that had so many toxic effects,
were no longer emphasized, and the failed idea of “essentiality”
was shifted to different categories of polyunsaturated fats.

The
addition of the long chain highly unsaturated fats to baby food formulas
was recently approved, on the basis of their supposed “essentiality
for brain development.” One of the newer arguments for the essentiality
of the PUFA is that “they are needed for making cell membranes.”
But human cells can grow and divide in artificial culture solutions
which contain none of the polyunsaturated fats, and no one has claimed
that they are growing “without membranes.”

The
long chain fats found in fish and some algae don't interfere with animal
enzymes as strongly as the seed oils do, and so by comparison, they
aren't so harmful. They are also so unstable that relatively little
of them is stored in the tissues. (And when they are used as food additives,
it's necessary to use antioxidants to keep them from becoming smelly
and acutely toxic.)

When
meat is grilled at a high temperature, the normally spaced double bonds
in PUFA migrate towards each other, becoming more stable, so that linoleic
acid is turned into “conjugated linoleic acid.” This analog of the
“essential” linoleic acid competes against the linoleic acid in
tissues, and protects against cancer, atherosclerosis, inflammation
and other effects of the normal PUFA. Presumably, anything which interferes
with the essential fatty acids is protective, when the organism contains
dangerous amounts of PUFA. Even the trans-isomers of the unsaturated
fatty acids (found in butterfat, and convertible into conjugated linoleic
acid) can be protective against cancer.

In
the 1980s the oil promoters were becoming more sophisticated, and were
publishing many experiments in which the fish oils were compared with
corn oil, or safflower, or soy oil, and in many of those experiments,
the animals' health was better when they didn't eat the very toxic seed
oils, that contained the “essential fatty acids,” linoleic and linoleic
acids.

Besides
comparing the fish oils to the stronger toxins, another trick is to
take advantage of the same immunosuppressive property that had seemed
troublesome, and to emphasize their ability to temporarily alleviate
some autoimmune or allergic diseases. X-rays were once used that way,
to treat arthritis and ringworm, for example.

And,
knowing that cancer cells have the ability to consume large amounts
of fatty acids, they would test these fats in tissue culture dishes,
and demonstrate that they were poisonous, cytotoxic, to the fast growing
cancer cells. Although they caused cancer in animals, if they could
be shown to kill cancer cells in a dish, they could be sold as anticancer
drugs/nutrients, with the special mystique of being “essential fatty
acids.” Strangely, their ability to kill cancer cells under some circumstances
and to suppress some immunological reactions is being promoted in close
association with the doctrine that these fats are nutritionally essential.

Arachidonic
acid is made from linoleic acid, and so those two oils were considered
as roughly equivalent in their ability to meet our nutritional needs,
but a large part of current research is devoted to showing the details
of how fish oils protect against arachidonic acid. The “balance”
between the omega -3 and the omega -6 fatty acids is increasingly being
presented as a defense against the toxic omega -6 fats. But the accumulation
of unsaturated fats with aging makes any defense increasingly difficult,
and the extreme instability of the highly unsaturated omega -3 fats
creates additional problems.

PUFA
and x-rays have many biological effects in common. They are immunosuppressive,
but they produce their own inflammatory reactions, starting with increased
permeability of capillaries, disturbed coagulation and proteolysis,
and producing fibrosis and tumefaction or tissue atrophy. This isn't
just a coincidence, since ionizing radiation attacks the highly unstable
polyunsaturated molecules, simply accelerating processes that ordinarily
happen more slowly as a result of stress and aging.

Prolonged
stress eventually tends to be a self-sustaining process, impairing the
efficient respiratory production of energy, converting muscle tissue
to amino acids, suppressing the thyroid, and activating further mobilization
of fatty acids. Fatty acids are mobilized from within the structure
of cells by phospholipases, and from fat tissues by other lipases.

The
highly unsaturated fatty acids, as well as the ordinary “essential
fatty acids,” act directly to increase capillary permeability, even
without conversion into prostaglandins, and they interfere in many ways
with the clotting and clot removal systems. The effects of PUFA taken
in a meal probably disturb the clotting system more than the same quantity
of saturated fat, contrary to many of the older publications. The PUFA
are widely believed to prevent clotting, but when cod liver oil is given
to “EFA deficient” animals, it activates the formation of clots
(Hornstra, et al., 1989). An opposite effect is seen when a long chain
fatty acid synergizes with aspirin, to restrain clotting (Molina, et
al., 2003).

Fibrosis
is a generalized consequence of the abnormal capillary permeability
produced by things that disrupt the clotting system. Estrogen, with
its known contribution to the formation of blood clots and edema and
fibrosis and tumors, achieves part of its effect by maintaining a chronically
high level of free fatty acids, preferentially liberating arachidonic
acid, rather than saturated fatty acids.

Butter,
beef fat, and lamb fat are the only mostly saturated fats produced on
a large scale in the U.S., and the cheapness/profitability of the seed
oils made it easy to displace them. But, in the face of the immense
amount of propagandistic “health” claims that have been made against
the saturated fats, it's instructive to look at some of their actual
effects, especially on the clotting system, and the related fibrotic
reactions.

The
saturated fatty acids are very unreactive chemically. Coconut oil, despite
containing about 1% of the unstable PUFA, can be left in a bucket at
room temperature for a year or more without showing any evidence of
deterioration, suggesting that the predominance of saturated fat acts
as an antioxidant for the unsaturated molecules. In the body, the saturated
fats seem to act the same way, preventing or even reversing many of
the conditions caused by oxidation of fats.

The
stress-induced liberation of arachidonic acid causes blood vessels to
leak, and this allows fibrin to escape from the blood stream, into the
basement membrane and beyond into the extracellular matrix, where it
produces fibrosis. (Cancer, autoimmune diseases, and heart disease involve
the same inflammatory, thrombotic, fibrotic processes as the nominal
fibroses.) Scleroderma, liver cirrhosis, fibrosis of the lungs, heart,
and other organs, and all the diseases in which fibrous tissue becomes
dense and progressively contracts, involve similar processes, and the
treatments which are successful are those that stop the inflammation
produced by the oxidation of the polyunsaturated fatty acids.

Retroperitoneal
fibrosis is now known to be produced by estrogen, and is treated by
antiestrogenic and antiserotonergic drugs, but as early as 1940 Alejandro
Lipschutz demonstrated that chronic exposure to very low doses of estrogen
produced fibromas in essentially every part of the body. Earlier, Loeb
had studied the action of large doses of estrogen, which produced fibrosis
of the uterus, as if it had accelerated aging. Following Lipschutz'
work, in which he demonstrated the “antifibromatogenic” actions
of pregnenolone and progesterone, several Argentine researchers showed
that progesterone prevented and cured abdominal adhesions and other
fibrotic conditions, including retroperitoneal fibrosis.

Since
estrogen produces both leakiness of the capillaries and excessive formation
of fibrin, its effects will be seen first in the organs where it concentrates,
but eventually anywhere capillaries leak fibrin. Estrogen activates
the phospholipase which liberates arachidonic acid, and progesterone
inhibits that phospholipase.

As
the fat tissues become more burdened with arachidonic acid, they release
it more easily in response to moderately lipolytic stress signals. This
could explain the increased levels of free fatty acids and lipid peroxidation
that occur with aging. In animals that are “deficient” in the polyunsaturated
fatty acids, adrenalin doesn't have the lipolytic effect that it does
in animals on the standard diet. With aging, there is not only a tendency
to have chronically higher free fatty acids in the blood, but for those
fatty acids to be more unsaturated. The phospholipids of mitochondria
and microsomes become more unsaturated with aging (Laganiere and Yu,
1993, Lee, et al., 1999). In the human retina there is a similar accumulation
of PUFA with aging (Nourooz-Zadeh and Pereira, 1999), which implies
that the aged retina will be more easily damaged by light.

Several
studies suggest that a high degree of unsaturation in the fats is fundamentally
related to the aging process, since long lived species have a lower
degree of unsaturation in their fats. Caloric restriction decreases
the age-related accumulation of the fatty acids with 4 and 5 double
bonds.

Although
publicity has emphasized the anti-inflammatory effects of fish oil,
experiments show that it is extremely effective in producing alcohol-related
liver cirrhosis. Breakdown products of polyunsaturated fats (isoprostanes
and 4-HNE) are found in the blood of people with alcoholic liver disease
(Aleynik, et al., 1998). In the absence of polyunsaturated fats, alcohol
doesn't produce cirrhosis. Saturated fats allow the fibrosis to regress:

In
these studies, the animals were switched from fish oil to either palm
oil or medium chain triglycerides (a major fraction of coconut oil).
In other studies, Knittel, et al. (1995), show that fibrinogen, in “a
clotting-like process,” is involved in the development of liver fibrosis,
and that this appears to provide a basis for the growth of additional
extracellular matrix.

The
relatively few studies of fish oil and linoleic acid that compare them
with palmitic acid or coconut oil have produced some very important
results. For example, pigs exposed to endotoxin developed severe lung
problems (resembling “shock lung”) when they had been on a diet
with either fish oil or Intralipid (which is mostly linoleic acid, used
for intravenous feeding in hospitals), but not after palmitic acid (Wolfe,
et al., 2002).

Eating
low-fat seafood (sole, whitefish, turbot, scallops, oysters, lobster,
shrimp, squid, etc.) once in a while can provide useful trace minerals,
without much risk. However, fish from some parts of the ocean contain
industrial contaminants in the fat, and large fish such as tuna, swordfish,
Chilean sea bass and halibut contain toxic amounts of mercury in the
muscles. Chilean sea bass (Patagonian toothfish) is very high in fat,
too.

About
ten years ago I met a young man with a degenerative brain disease, and
was interested in the fact that he (working on a fishing boat) had been
eating almost a pound of salmon per day for several years. There is
now enough information regarding the neurotoxic effects of fish oil
to justify avoidance of the fatty fish.

Some
of the current advertising is promoting fish oil to prevent cancer,
so it's important to remember that there are many studies showing that
it increases cancer.

The
developmental and physiological significance of the type of fatty acid
in the diet has been established for a long time, but cultural stereotypes
and commercial interests are threatened by it, so it can't be discussed
publicly.

Obstet Gynecol. 1987 Sep;70(3 Pt 2):502-4. The treatment of retroperitoneal
fibromatosis with medroxyprogesterone acetate. Barnhill D, Hoskins
W, Burke T, Weiser E, Heller P, Park R. Wide excision is the recommended
primary therapy for retroperitoneal fibromatosis. Radiation therapy
and a variety of medications have been used to treat patients with recurrent
tumors, but the response to these agents has not been uniform. The patient
presented was successfully treated with medroxyprogesterone acetate
for recurrent retroperitoneal fibromatosis that was refractory to multiple
operative resections and radiation therapy.

Dtsch Med Wochenschr. 2003 Jun 20;128(25-26):1395-8. [Rare
cause of chronic abdominal pain: retractile mesenteritis] [in German]
Hermann F, Speich R, Schneemann M. “Retractile mesenteritis is a rare
cause of chronic abdominal pain with variable symptoms. Its aetiology
is unknown. In case of bowel ischemia a surgical approach is preferred,
milder forms may be treated with immunosuppressive agents as well as
oral progesterone. Progesterone has exhibited positive effects on fatty
tissue with successful treatment in desmoid tumors and retroperitoneal
fibrosis. Here in we could demonstrate its safe and efficient use in
a patient with retractile mesenteritis.”

Mech Ageing
Dev 2001 Apr 15;122(4):427-43. Effect of the degree of fatty
acid unsaturation of rat heart mitochondria on their rates of H2O2 production
and lipid and protein oxidative damage. Herrero A, Portero-Otin
M, Bellmunt MJ, Pamplona R, Barja G. “Previous comparative studies
have shown that long-lived animals have lower fatty acid double bond
content in their mitochondrial membranes than short-lived ones. In order
to ascertain whether this trait protects mitochondria by decreasing
lipid and protein oxidation and oxygen radical generation, the double
bond content of rat heart mitochondrial membranes was manipulated by
chronic feeding with semi-purified AIN-93G diets rich in highly unsaturated
(UNSAT) or saturated (SAT) oils. UNSAT rat heart mitochondria had significantly
higher double bond content and lipid peroxidation than SAT mitochondria.
They also showed increased levels of the markers of protein oxidative
damage malondialdehyde-lysine, protein carbonyls, and N(e)-(carboxymethyl)lysine
adducts.” “These results demonstrate that increasing the degree
of fatty acid unsaturation of heart mitochondria increases oxidative
damage to their lipids and proteins, and can also increase their rates
of mitochondrial oxygen radical generation in situations in which the
degree of reduction of Complex III is higher than normal. These observations
strengthen the notion that the relatively low double bond content of
the membranes of long-lived animals could have evolved to protect them
from oxidative damage.”

Biochem J. 1994 May 15;300 ( Pt 1):251-5. Regulation of fibrinolysis
by non-esterified fatty acids. Higazi AA, Aziza R, Samara AA, Mayer
M. “Examination of the fatty acid specificity showed that a minimal
chain length of 16 carbon atoms and the presence of at least one double
bond, preferably in a cis configuration, were required for inhibition
of the fibrinolytic activity of plasmin.”

Science. 1976 Feb 27;191(4229):861-2. Nicotinic acid reduction of
plasma volume loss after thermal trauma. Hilton JG, Wells CH. Intravenous
administration of nicotinic acid to the anesthetized dog prior to thermal
trauma reduced plasma loss at 10 minutes after burn from 7 milliliters
per kilogram to less than 2 millimeters per kilogram. During the next
50 minutes plasma loss was the same in treated and untreated animals.
An additional dose of nicotinic acid 30 minutes after burn prevented
this further loss.

Nutr
Cancer. 1985;7(4):199-209. Isomeric fatty acids and tumorigenesis:
a commentary on recent work. Hunter JE, Ip C, Hollenbach EJ. “Neither
epidemiological nor experimental studies published to date have demonstrated
any valid association between trans fatty acid ingestion and tumorigenesis.
A recent study showed that under controlled conditions, a fat with a
high content of trans fatty acids did not promote the development of
mammary tumors induced in rats by 7,12-dimethylbenz[a]anthracene to
any greater extent than did a comparable fat with a high content of
cis fatty acids. In addition, in this study a high trans fat was
less tumor promoting than was a blend of fats that simulated the dietary
fat composition of the United States and had a lower level of trans
fatty acids.”

Folia
Haematol Int Mag Klin Morphol Blutforsch. 1977;104(1):1-10. [Review:
hemorrhagic diathesis resulting from acute exposure to ionizing Radiation]
[Article in German] Krantz S, Lober M. The symptoms of the acute radiopathy
are chiefly characterized by a severe blood coagulation disorder. The
main results and problems of research work on this haemorrhagic diathesis
are shortly reviewed.

Acta Chir Scand. 1976;142(1):20-5. Induction of endogenous fibrinolysis
inhibition in the dog. Effect of intravascular coagulation and release
of free fatty acids. Lindquist O, Bagge L, Saldeen T. “In all
groups subjected to infusion of thrombin an increase in plasma free
fatty acids (FFA) was observed. The role of this increase for the development
of fibrinolysis inhibition was tested by infusion of norepinephrine
alone and in combination with nicotinic acid. Norepinephrine caused
an increase of FFA after 2 hours and in urokinase inhibitor activity
after 24-48 hours. Both of these were diminished by high doses of
nicotinic acid, indicating that the release of FFA rather than intravascular
coagulation might be the principal mechanism underlying the occurrence
of fibrinolysis inhibition following trauma.”

J Biochem (Tokyo). 1977 Aug;82(2):529-33. Effects of free fatty acids
on fibrinolytic activity. Muraoka T, Okuda H. A novel method for
the estimation of fibrinolytic activity is proposed. In this method,
a fibrin clot suspension is used as a substrate (fibrin is known to
be a physiological substrate of plasmin). The fibrin clot suspension
was prepared by homogenization of human fibrin clots. With this method,
we found that free fatty acids inhibited the plasmin activity, and
long-chain, unsaturated free fatty acids had a particularly strong inhibitory
action on plasmin. As regards the mechanism of the inhibitory action,
free fatty acids may not inhibit complex formation between plasmin and
fibirin, but may make it impossible for plasmin to act on fibrin due
to deformation of the surface of the fibrin clot.

Radiobiologiia.
1985 Nov-Dec;25(6):763-7. [Mechanism of circulatory disorders in
animals irradiated at high doses] [in Russian] Pozharisskaia TD,
Vasil'eva TP, Sokolova EN, Alekseeva II. Some data are reported on pathoanatomical
changes, a status of the microcirculatory channel and the coagulogram
of animals affected by high doses of ionizing radiation. The signs
of disseminated intravascular blood coagulation have been revealed.

Nutr Cancer 1995;24(1):33-45.
Effects of linoleic acid and gamma-linolenic acid on the growth and
metastasis of a human breast cancer cell line in nude mice and on its
growth and invasive capacity in vitro. Rose DP, Connolly JM, Liu
XH

Nutr Cancer 1998;30(2):137-43.
Effects of dietary n-3-to-n-6 polyunsaturated fatty acid ratio on mammary
carcinogenesis in rats. Sasaki T, Kobayashi Y, Shimizu J, Wada M,
In'nami S, Kanke Y, Takita T. “An increase in the n-3/n-6 ratio did
not suppress the incidence or reduce the latency of mammary tumor development.
The number and weight of mammary tumors per tumor-bearing rat tended
to be large in the group with an n-3/n-6 ratio of 7.84 compared with
those in the other groups. As the n-3/n-6 ratios were elevated, the
total number and weight of tumors increased gradually.”

Ups
J Med Sci. 1979;84(3):195-201. Effect of nicotinic acid on the posttraumatic
increase in free fatty acids and fibrinolysis inhibition activity in
the rat. Wegener T, Bagge L, Saldeen T. Nicotinic acid effectively
inhibited the posttraumatic increase in both free fatty acids (FFA)
and fibrinolysis inhibition activity (FIA) in the blood in rats, indicating
that FFA might be involved in the posttraumatic increase of FIA. The
FIA in the liver was greater than that in other organs studied and was
increased in the posttraumatic phase. The possible role of the liver
in the posttraumatic increase of FIA is discussed.